传染病信息
傳染病信息
전염병신식
INFECTIOUS DISEASE INFORMATION
2013年
6期
358-361
,共4页
肝炎,乙型,慢性%核苷类%糖皮质激素
肝炎,乙型,慢性%覈苷類%糖皮質激素
간염,을형,만성%핵감류%당피질격소
hepatitis B,chronic%nucleosides%glucocorticoids
目的：回顾性分析因免疫性基础疾病等使用糖皮质激素的慢性HBV感染者，应用核苷类药物预防治疗HBV再激活及免疫性疾病活动的临床效果。方法随机选取131例HBV感染并因免疫性疾病应用糖皮质激素治疗的患者，分为3组：A组41例，血清ALT正常，HBV DNA载量≤1×103 copies/ml；B组67例，ALT＜2倍正常值上限（upper limits of normal, ULN），1×103 copies/ml＜HBV DNA载量＜1×104 copies/ml；C组23例，ALT≥2×ULN，HBV DNA载量≥1×104 copies/ml，应用拉米夫定、恩替卡韦或拉米夫定+阿德福韦酯治疗，每3个月随访HBV DNA载量和ALT水平。结果口服核苷类药物可明显抑制病毒复制，有利于控制免疫性疾病活动。如不给予核苷类药物治疗，当HBV DNA载量>1×103 copies/ml时HBV DNA复制和免疫性疾病活动风险更高。但无论病毒载量高低，采用单药拉米夫定/恩替卡韦，或拉米夫定+阿德福韦酯均出现良好应答。对拉米夫定单药或加用阿德福韦酯应答不良者，恩替卡韦治疗仍可获得理想应答。结论因免疫性疾病采用糖皮质激素治疗的患者，无论HBV DNA载量是否高于正常值，均应给予核苷类药物治疗，且应尽早使用强效、低耐药的药物。
目的：迴顧性分析因免疫性基礎疾病等使用糖皮質激素的慢性HBV感染者，應用覈苷類藥物預防治療HBV再激活及免疫性疾病活動的臨床效果。方法隨機選取131例HBV感染併因免疫性疾病應用糖皮質激素治療的患者，分為3組：A組41例，血清ALT正常，HBV DNA載量≤1×103 copies/ml；B組67例，ALT＜2倍正常值上限（upper limits of normal, ULN），1×103 copies/ml＜HBV DNA載量＜1×104 copies/ml；C組23例，ALT≥2×ULN，HBV DNA載量≥1×104 copies/ml，應用拉米伕定、恩替卡韋或拉米伕定+阿德福韋酯治療，每3箇月隨訪HBV DNA載量和ALT水平。結果口服覈苷類藥物可明顯抑製病毒複製，有利于控製免疫性疾病活動。如不給予覈苷類藥物治療，噹HBV DNA載量>1×103 copies/ml時HBV DNA複製和免疫性疾病活動風險更高。但無論病毒載量高低，採用單藥拉米伕定/恩替卡韋，或拉米伕定+阿德福韋酯均齣現良好應答。對拉米伕定單藥或加用阿德福韋酯應答不良者，恩替卡韋治療仍可穫得理想應答。結論因免疫性疾病採用糖皮質激素治療的患者，無論HBV DNA載量是否高于正常值，均應給予覈苷類藥物治療，且應儘早使用彊效、低耐藥的藥物。
목적：회고성분석인면역성기출질병등사용당피질격소적만성HBV감염자，응용핵감류약물예방치료HBV재격활급면역성질병활동적림상효과。방법수궤선취131례HBV감염병인면역성질병응용당피질격소치료적환자，분위3조：A조41례，혈청ALT정상，HBV DNA재량≤1×103 copies/ml；B조67례，ALT＜2배정상치상한（upper limits of normal, ULN），1×103 copies/ml＜HBV DNA재량＜1×104 copies/ml；C조23례，ALT≥2×ULN，HBV DNA재량≥1×104 copies/ml，응용랍미부정、은체잡위혹랍미부정+아덕복위지치료，매3개월수방HBV DNA재량화ALT수평。결과구복핵감류약물가명현억제병독복제，유리우공제면역성질병활동。여불급여핵감류약물치료，당HBV DNA재량>1×103 copies/ml시HBV DNA복제화면역성질병활동풍험경고。단무론병독재량고저，채용단약랍미부정/은체잡위，혹랍미부정+아덕복위지균출현량호응답。대랍미부정단약혹가용아덕복위지응답불량자，은체잡위치료잉가획득이상응답。결론인면역성질병채용당피질격소치료적환자，무론HBV DNA재량시부고우정상치，균응급여핵감류약물치료，차응진조사용강효、저내약적약물。
Objective To retrospectively analyze the therapeutic efficacy of nucleoside analogues on HBV reactivation and activation of underlying immune diseases in chronically HBV-infected patients receiving glucocorticoid therapy due to underlying immune diseases. Methods A total of 131 HBV-infected patients receiving glucocorticoid therapy due to underlying immune diseases were enrolled in the study. They were divided into 3 groups according to the serum levels of HBV DNA and ALT. There were 41 patients in group A with normal serum level of ALT and HBV DNA ≤1×103 copies/ml, 67 patients in group B with ALT less than twice upper limits of normal (ULN) and HBV DNA >1 ×103 copies/ml but <1 ×104 copies/ml, and 23 patients in group C with ALT no less than twice ULN and HBV DNA ≥1 ×104 copies/ml. Antiviral treatment strategies included lamivudine (LAM) therapy, entecavir (ETV) therapy or LAM+adefovir dipivoxil (ADV) therapy. The serum levels of HBV DNA and ALT were detected every 3 months. Results Oral administration of nucleoside analogues could inhibit viral replication significantly, and helped control the activation of underlying immune diseases. If nucleoside analogue therapy was not given, the patients with HBV DNA>1 ×103 copies/ml would be at higher risk for viral replication and the activation of underlying immune diseases. However, regardless of the level of HBV DNA, the patients showed good response to LAM, ETV or LAM+ADV. Those who didn't respond well to LAM or LAM+ADV might obtain good response to ETV. Conclusions Patients receiving glucocorticoid therapy due to underlying immune diseases, regardless of the level of HBV DNA, should be given nucleoside analogue therapy, and early use of antiviral agents with high effectiveness and low drug resistance is recommended.
